painless thyroiditis
Introduction
Introduction to painless thyroiditis Painless thyroiditis (PT), also known as silent thyroiditis (ST), is a special type of thyroiditis. In 1971, Hamburger first described a case called "potential subacute thyroiditis." Since then, more and more scholars have reported such cases, and admitted that this is an independent disease, ST has the common features of subacute thyroiditis and chronic lymphocytic thyroiditis, but not identical. In recent years, it has been classified as subacute thyroiditis, called subacute lymphocytic thyroiditis, to distinguish subacute granulomatous thyroiditis (commonly known as subacute thyroiditis). In addition, the disease also has subacute non-suppurative thyroiditis, postpartum painless thyroiditis and other names. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: hypothyroidism
Cause
Causes of painless thyroiditis
Environmental factors (25%):
It has been reported that PT occurs after viral infection. Epidemiological studies have shown that PT is related to geographical, environmental and seasonal factors. It is a destructive thyroiditis. Viral infection causes inflammatory damage of thyroid follicular cells, releasing T3, T4 causes hyperthyroidism, and thyroid gland. It is painless and painless, and may be caused by a new virus strain or by different individuals reacting to the same virus.
Autoimmune (20%):
A special type of chronic lymphocytic thyroiditis is considered to be an autoimmune disease. It has been reported that patients with HLA-DR3 and DR5 are susceptible to PT, and some patients have elevated TGAb and TPOAb titers (about 50%), TSAb ( Positive for thyroid stimulating antibodies (10%), pathological examination showed lymphocytic thyroid-like changes.
Disease infection (20%):
It is believed that a special type of thyroiditis virus infection (with its geographical and seasonal) caused by the combination of viral infection and autoimmune reaction is the cause of the disease, resulting in different degrees of cellular immune response and certain specific individuals (such as HLA-DR3 and DR5, etc.) produce autoimmune antibodies.
For postpartum thyroiditis, some people think that it may be a pre-existing subclinical thyroid autoimmune disease. After the postpartum, the immune mechanism of the body is weakened, the disease develops into the clinical stage by itself, and the autoimmune thyroid disease is in the early 3 months of pregnancy. Within, the anti-thyroid antibody titer may be high, but the antibody titer drops to disappear in the middle and late pregnancy, and a temporary "immune rebound" can occur after delivery, the antibody titer returns to pre-pregnancy levels, and even more High, or transient antibody in postpartum, this immune rebound is a strong stimulus for sensitive individuals, may cause the disease to develop or relapse.
PT and other autoimmune diseases, such as type I diabetes, autoimmune hemolytic anemia, systemic lupus erythematosus, rheumatoid arthritis, etc. coexist or occur, also confirmed that it is an autoimmune disease, some patients measured Serum levels of interleukin 12 (IL-12) and interleukin 5 (IL-5) were measured in a helper T-type immune response (Th1-type) in autoimmune thyroid disease, and patients were found to have significantly higher serum IL-12 levels. In the normal control group and subacute thyroiditis combined with hyperthyroidism, the ratio of IL-12 to IL-5 was also significantly higher in patients with normal control and Graves disease, IL-5 in patients with Graves disease and chronic lymphocytic thyroiditis. The serum was significantly elevated, but not elevated in PT, indicating that the pathogenesis of PT is a Th1-type immune response.
The relationship between genetic factors and environmental factors (such as high iodine diet) and ST has been reported in recent years, but it is limited to research reports on some related factors.
Pathogenesis
Pathogenesis
The autoimmune reaction damages the thyroid follicular cells, the thyroid iodine function decreases, and the gel overflows, so that the stored thyroxine is released into the blood and the symptoms of hyperthyroidism appear. As the inflammatory process progresses, the stored thyroid hormone is depleted, and the thyroid gland is absent. Ability to synthesize new thyroid hormones, hyperthyroidism symptoms are relieved or disappeared, about half of the patients have clinical hypothyroidism or laboratory hypothyroidism, TSH is elevated, serum T3, T4 titers are reduced, and the damage is restored as the thyroid inflammation subsides The 131I absorption rate can be changed to normal or higher than normal, TSH returns to normal, the thyroid gland produces and releases new hormones, and the condition resolves itself.
2. Pathological changes
In all specimens, lymphocytic infiltration is a common manifestation, and follicular cell destruction and fibrosis similar to subacute thyroiditis can be seen, but the characteristics of foreign body giant cells and Hashimoto's thyroiditis are less common. The germinal center changed.
Prevention
Painless thyroiditis prevention
To prevent painless thyroiditis, we must start with life. First of all, we must maintain the peace of mind, but also work and rest, and develop regular living habits.
1. Maintain the peace of mind. People's spirit and body have a lot to do, to maintain the comfort of the spirit, to prevent bad mental stimulation can prevent thyroiditis. Clinically, patients with thyroiditis often have adverse stimuli before their condition worsens. If you are arguing with colleagues and family members because of a small matter, you cannot control yourself. Therefore, patients must learn to control their emotions. Colleagues from family and units should understand the patient and create a better environment.
2, work and rest, develop a regular habits. Healthy people can't think that their health is good, they stay up all night. Although the patient eats a lot, the digestion and absorption function is poor and the body is weak. Generally speaking, light people should not stay up late and perform strenuous activities such as long-distance running, swimming, climbing, etc. Those who are seriously ill should stay still and even rest in bed. In addition, because thyroiditis patients often accompanied by exophthalmia, extraocular muscle paralysis, prone to visual fatigue, eye pain.
Complication
Painless thyroiditis complications Complications hypothyroidism
A small percentage of patients may have permanent hypothyroidism.
Symptom
Painless symptoms of thyroiditis Common symptoms Postpartum thyroid enlargement Goiter palpitations ESR increased fast thyroid enlargement Mucinous edema Nodules Weight loss Attention deficit
The typical clinical course can be divided into 4 stages: thyrotoxicosis (early stage), normal thyroid function, hypothyroidism (hypothyroidism) and recovery period, but half of the patients have no hypothyroidism and only the first two phases .
1. Thyrotoxicosis:
The main clinical manifestation is the symptoms of hyperthyroidism caused by thyroid hormone spillage after thyroid follicular destruction. The onset of the disease is sudden. The general systemic symptoms are not different from those of other diseases. The clinical features are as follows:
(1) There is no prodromal symptoms of viral infection before onset, no history of iodine exposure.
(2) usually manifested as mild or moderate hyperthyroidism, about 10% of patients may have a high metabolic state, generally no exophthalmos, about 80% of patients without any clinical symptoms.
(3) No fever, about 50% of patients with increased erythrocyte sedimentation rate.
(4) About half of the patients have goiter, and a few may be associated with nodules.
(5) The thyroid is painless and no tender, and is a prominent feature of ST.
(6) Mucinous edema before innocent.
(7) Serum T3, T4, FT3, FT4 can be increased, and TSH is decreased.
(8) The absorption rate of thyroid 131I was significantly decreased and delayed, especially the absorption rate of 24h was below 3%, and it did not rise after administration of thyroxine.
(9) About 50% of patients have diffuse or focal lymphocytic infiltration, tissue fibrosis and Hurthle cells are rare, and no granuloma changes in subacute inflammation.
(10) Increased urinary iodine content.
2. Normal thyroid function:
ST patients generally have symptoms relieved within 2 to 6 months, serum T3, T4 decreased, 131I absorption rate increased to normal levels, hyperthyroidism symptoms subsided, this period can last for several weeks.
3. Hypothyroidism:
About 1/4 to 1/3 of patients with serum T3, T4 can be progressively decreased with hypothyroidism, TSH increased, this period can last 1 to 6 months, usually no more than 1 year, clinical hypothyroidism, light They can relieve themselves in a short period of time, and rarely develop permanent hypothyroidism.
4. Recovery period:
The clinical symptoms disappeared, serum thyroid hormone levels and 131I absorption rate returned to normal, and some patients directly entered the recovery period without undergoing hypothyroidism.
The clinical manifestations of postpartum patients are often short-lived and vague, with obvious individual differences. Patients often have hyperthyroidism 1 to 6 months postpartum, and the onset is more urgent. It is characterized by postpartum transient, painless, diffuse or Nodular goiter, hyperthyroidism, light weight, mainly weight loss, obvious fatigue, palpitations, increased appetite and nervous system symptoms, such as heat, sweating, nervousness, anxiety, inattention, memory loss, serum T3, T4, FT3, FT4 increased, TSH decreased, 131I absorption rate decreased, more than 80% of patients were positive for TPOAb, and about 1/3 of TGAb positive patients, only 40% of patients had characteristic thyroid function evolution, 60% The cases were only in the hyperthyroidism stage. After treatment, the patients directly transitioned to the recovery period. Patients without thyroid function changes often had only painless goiter. The recurrence rate of postpartum ST patients with re-pregnancy was as high as 50%.
Examine
Painless thyroiditis
1. Thyroid function test: In the early stage of the disease, with the destruction of thyroid follicles, T3 and T4 in the blood circulation are significantly increased, serum thyroglobulin is elevated, T3/T4<20:1 (ng/g), and some authors believe that FT3 /FT4 determination <0.24 (nmol/nmol) can more objectively reflect the thyroid function in painless thyroiditis as a basis for diagnosis.
2. Erythrocyte sedimentation rate: normal or mildly elevated early in the disease, which is significantly different from subacute thyroiditis.
3.131I uptake rate check: Thyroid 131I uptake rate decreased, TSH stimulation can not increase it.
4. Thyroglobulin antibodies and microsomal antibody tests: Positive in half of patients.
5. Histopathological examination: needle biopsy, manifested as diffuse or focal lymphocytic infiltration, no granuloma changes, no fibrosis seen in Hashimoto's thyroiditis, no germinal center formation or rare.
Diagnosis
Diagnosis and identification of painless thyroiditis
diagnosis
Any woman who has fatigue, palpitations, mood swings or goiter within 1 year after birth should be suspected of having postpartum thyroiditis. For middle-aged people, there is painless goiter and hyperthyroidism, and Serum T3, T4 increased, 131 iodine rate decreased in the thyroid, should consider this disease.
Differential diagnosis
1. Subacute thyroiditis: subacute thyroiditis rarely occurs hyperthyroidism, thyroid pain and tenderness; while painless thyroiditis does not cause thyroid pain or tenderness; subacute thyroiditis with hyperthyroidism rarely recurs; And 10% to 15% of painless thyroiditis can be recurrent, viral infection prodromal symptoms are common in subacute thyroiditis; rarely seen in painless thyroiditis, subacute thyroiditis most erythrocyte sedimentation rate, up to 100mm / 1h The painless thyroid gland only mildly increased.
2.Graves hyperthyroidism: Graves hyperthyroidism T3, T4 value increased, the rate of 131I increased, while painless thyroiditis, T3, T4 increased, T3/T4<20:1, FT3/FT4<0.24, 131I rate Reduced (usually <3%), no exudation and sputum mucinous edema, the course of the disease is as short as several weeks or months.
3. Chronic lymphocytic thyroiditis: Although the symptoms of hyperthyroidism are the same, the rate of 131I in chronic lymphocytic thyroiditis is still high or higher than normal. The symptoms of hyperthyroidism are rarely relieved naturally. The needle biopsy can be used for identification. Diagnostic significance.
4. Identification of other diseases reduced by 131I: identification of iodothyroid, drug-induced hyperthyroidism, metastatic functional thyroid cancer.
5 postpartum PT: should also pay attention to the lack of thyroid hormone to cause pituitary pseudoadenomatous hyperprolactin hyperemia and true postpartum prolactinoma differentiation, long-term amenorrhea caused by postpartum thyroid dysfunction should be combined with Xi Han Identification of autoimmune pituitary inflammation.
